The search for tools that increase the effectiveness of cell therapy of demyelinating pathology is relevant. They may be preparations that affect the pathogenetic factors of this pathology, in particular, the pineal hormone melatonin.The purpose of the work is to evaluate the involvement of immune system and antioxidant defense in the implementation of the protective effects of melatonin on morpho-functional disorders in the central nervous system induced by neurotoxin cuprizone.Materials and methods. The toxic demyelination model was induced on 129/Sv mice at the age of 3-5 months by adding cuprizone to food for 3 weeks. Since the 7th day of cuprizone administration, melatonin was injected intraperitoneally at 18:00 daily, at a dose of 1 mg/kg. In the brain of mice, the proportion of CD3+, Nestin+ cells and phagocytic macrophages, the content of malondialdehyde and the activity of antioxidant enzymes was determined. Blood serum was tested for thymic hormone thymulin levels. In the animals, we evaluated the structure of the brain and spinal cord neurons by Nissl staining of histological sections as well as analyzed behavioural reactions in the "open field" test.Results. In the brain of the mice received cuprizone, the proportion of CD3+ and Nestin+ cells, active macrophages and malondialdehyde content increases, glutathione peroxidase and glutathione reductase levels decreases. In the brain and spinal cord of the mice with a cuprizone diet, the proportion of altered neurons increases, and motor and emotional activity decreases. The introduction of melatonin results in a decrease in the relative number of CD3+ cells, active macrophages and malondialdehyde content, increased activity of glutathione peroxidase, glutathione reductase and level of thymulin. In such mice, the proportion of unchanged neurons increases as the number of Nestin+ cells decreases and behavioural responses are also improved.Conclusions. The neuroprotective effect of melatonin in demyelinating pathology is realized through the factors of the immune system and oxidative stress. The results may be useful in the development of new biotechnological approaches to the treatment of demyelinating pathology, in particular, multiple sclerosis.
Functional Expression of the New Gap Junction Gene Connexin47 Transcribed in Mouse Brain and Spinal Cord Neurons
